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Characterization of factors antagonizing the PIE-1- and NuRD complex-involved SynMuv pathways in C. elegans Export

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caenorhabditis_elegans celegans c_elegans elegans lag-2 meeting_abstract nematode pgl-1 wormbase y73c8b4 zk3814

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As embryogenesis progresses, developmental potentials become rapidly restricted in somatic cells while germ cells appear to maintain the existing totipotency. Recent evidence suggests that a nucleosome remodeling (NuRD) complex containing LET-418, HDA-1, and MEP-1 mediates the inactivation of germline potential in somatic cells of the C. elegans embryo. In the germline, the NuRD complex activity appears to be inhibited by PIE-1, a germline-specific zinc-finger protein, which directly interacts with the NuRD complex. We propose that this repression of the complex function is pivotal for the maintenance of the unique chromatin organization in the germline and thereby for the inhibition of somatic differentiation in these cells. In order to identify factors, we performed a genetic screen to search for genes which mediating the interaction of PIE-1 and the NuRD complex. We have screened 20,000 mutagenized haploid genomes and isolated 73 mutants that show strong suppression of the SynMuv caused by PIE-1 expression. These mutants can be categorized into several distinct classes based on the phenotypes such as vulval induction of synMuv B genes, RNAi sensitivity, germline- and somatic transgene silencing, and tissue specific expression of pgl-1 and lag-2 genes. Among those, ex109 and ex120 alleles were mapped on LGIV and used to further characterize their roles on antagonizing the PIE-1- and NuRD complex-induced SynMuv pathways in C. elegans.


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